Zobrazeno 1 - 10
of 20
pro vyhledávání: '"Veronica Zorzi"'
Autor:
Fabiola Paciello, Veronica Zorzi, Marcello Raspa, Ferdinando Scavizzi, Claudio Grassi, Fabio Mammano, Anna Rita Fetoni
Publikováno v:
Frontiers in Cell and Developmental Biology, Vol 10 (2022)
Pathogenic mutations in the Gjb2 and Gjb6 genes, encoding connexin 26 (Cx26) and connexin 30 (Cx30), respectively, have been linked to the most frequent monogenic hearing impairment, nonsyndromic hearing loss, and deafness DFNB1. It is known that Cx2
Externí odkaz:
https://doaj.org/article/19f4a25f91094337b5b74ffd5654ba8d
Autor:
Giulia Gentile, Fabiola Paciello, Veronica Zorzi, Antonio Gianmaria Spampinato, Maria Guarnaccia, Giulia Crispino, Abraham Tettey-Matey, Ferdinando Scavizzi, Marcello Raspa, Anna Rita Fetoni, Sebastiano Cavallaro, Fabio Mammano
Publikováno v:
Frontiers in Cell and Developmental Biology, Vol 8 (2021)
Pathogenic mutations in the non-syndromic hearing loss and deafness 1 (DFNB1) locus are the primary cause of monogenic inheritance for prelingual hearing loss. To unravel molecular pathways involved in etiopathology and look for early degeneration bi
Externí odkaz:
https://doaj.org/article/3f5c1a6757a44493910d53641e31af12
Autor:
Anna Rita Fetoni, Veronica Zorzi, Fabiola Paciello, Gaia Ziraldo, Chiara Peres, Marcello Raspa, Ferdinando Scavizzi, Anna Maria Salvatore, Giulia Crispino, Gabriella Tognola, Giulia Gentile, Antonio Gianmaria Spampinato, Denis Cuccaro, Maria Guarnaccia, Giovanna Morello, Guy Van Camp, Erik Fransen, Marco Brumat, Giorgia Girotto, Gaetano Paludetti, Paolo Gasparini, Sebastiano Cavallaro, Fabio Mammano
Publikováno v:
Redox Biology, Vol 19, Iss , Pp 301-317 (2018)
Mutations in GJB2, the gene that encodes connexin 26 (Cx26), are the most common cause of sensorineural hearing impairment. The truncating variant 35delG, which determines a complete loss of Cx26 protein function, is the prevalent GJB2 mutation in se
Externí odkaz:
https://doaj.org/article/4157f176ca6c433d98c82de45af9277e
Autor:
Giulia Crispino, Fabian Galindo Ramirez, Matteo Campioni, Veronica Zorzi, Mark Praetorius, Giovanni Di Pasquale, John A. Chiorini, Fabio Mammano
Publikováno v:
Scientific Reports, Vol 7, Iss 1, Pp 1-13 (2017)
Abstract We have previously shown that in vitro transduction with bovine adeno–associated viral (BAAV) vectors restores connexin expression and rescues gap junction coupling in cochlear organotypic cultures from connexin–deficient mice that are m
Externí odkaz:
https://doaj.org/article/f5b21be5ccfe4f96b4c632312c5f3207
Autor:
Veronica Zorzi, Fabiola Paciello, Gaia Ziraldo, Chiara Peres, Flavia Mazzarda, Chiara Nardin, Miriam Pasquini, Francesco Chiani, Marcello Raspa, Ferdinando Scavizzi, Andrea Carrer, Giulia Crispino, Catalin D. Ciubotaru, Hannah Monyer, Anna R. Fetoni, Anna M. Salvatore, Fabio Mammano
Publikováno v:
Frontiers in Molecular Neuroscience, Vol 10 (2017)
Panx1 forms plasma membrane channels in brain and several other organs, including the inner ear. Biophysical properties, activation mechanisms and modulators of Panx1 channels have been characterized in detail, however the impact of Panx1 on auditory
Externí odkaz:
https://doaj.org/article/4d42535be1534126b19e30919e612212
Autor:
Liang Xu, Andrea Carrer, Francesco Zonta, Zhihu Qu, Peixiang Ma, Sheng Li, Federico Ceriani, Damiano Buratto, Giulia Crispino, Veronica Zorzi, Gaia Ziraldo, Francesca Bruno, Chiara Nardin, Chiara Peres, Flavia Mazzarda, Anna M. Salvatore, Marcello Raspa, Ferdinando Scavizzi, Youjun Chu, Sichun Xie, Xuemei Yang, Jun Liao, Xiao Liu, Wei Wang, Shanshan Wang, Guang Yang, Richard A. Lerner, Fabio Mammano
Publikováno v:
Frontiers in Molecular Neuroscience, Vol 10 (2017)
Background: Mutations leading to changes in properties, regulation, or expression of connexin-made channels have been implicated in 28 distinct human hereditary diseases. Eight of these result from variants of connexin 26 (Cx26), a protein critically
Externí odkaz:
https://doaj.org/article/cc3dd804c27e4ae68e8efa44292bdd38
Autor:
Giulia, Gentile, Fabiola, Paciello, Veronica, Zorzi, Antonio Gianmaria, Spampinato, Maria, Guarnaccia, Giulia, Crispino, Abraham, Tettey-Matey, Ferdinando, Scavizzi, Marcello, Raspa, Anna Rita, Fetoni, Sebastiano, Cavallaro, Fabio, Mammano
Publikováno v:
Frontiers in Cell and Developmental Biology
Pathogenic mutations in the non-syndromic hearing loss and deafness 1 (DFNB1) locus are the primary cause of monogenic inheritance for prelingual hearing loss. To unravel molecular pathways involved in etiopathology and look for early degeneration bi
Autor:
Flavia, Mazzarda, Annunziata, D'Elia, Roberto, Massari, Adele, De Ninno, Francesca Romana, Bertani, Luca, Businaro, Gaia, Ziraldo, Veronica, Zorzi, Chiara, Nardin, Chiara, Peres, Francesco, Chiani, Abraham, Tettey-Matey, Marcello, Raspa, Ferdinando, Scavizzi, Alessandro, Soluri, Anna Maria, Salvatore, Jun, Yang, Fabio, Mammano
Publikováno v:
Lab on a chip. 20(16)
Prior work supports the hypothesis that ATP release through connexin hemichannels drives spontaneous Ca2+ signaling in non-sensory cells of the greater epithelial ridge (GER) in the developing cochlea; however, direct proof is lacking. To address thi
Autor:
Yu Li, Flavia Mazzarda, Lili Liu, Damiano Buratto, Francesco Zonta, Richard A. Lerner, Fabio Mammano, Marcello Raspa, Francesco Chiani, Youjun Chu, Gaia Ziraldo, Min Qiang, Ferdinando Scavizzi, Xiaojie Shi, Yaru Shi, Yuanyuan Kuang, Anna Maria Salvatore, Chiara Nardin, Guang Yang, Veronica Zorzi, Chiara Peres
Publikováno v:
EBioMedicine
Background Numerous currently incurable human diseases have been causally linked to mutations in connexin (Cx) genes. In several instances, pathological mutations generate abnormally active Cx hemichannels, referred to also as "leaky" hemichannels. T
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::e5a79dd8ad793aeabb5d22c5e0801622
http://hdl.handle.net/11577/3346805
http://hdl.handle.net/11577/3346805
Autor:
Fabio Mammano, Veronica Zorzi, Gaia Ziraldo, Giovanna Morello, Anna Maria Salvatore, Maria Guarnaccia, Anna Rita Fetoni, Gaetano Paludetti, Denis Cuccaro, Guy Van Camp, Giulia Gentile, Fabiola Paciello, Marco Brumat, Antonio Gianmaria Spampinato, Erik Fransen, Giulia Crispino, Chiara Peres, Sebastiano Cavallaro, Ferdinando Scavizzi, Gabriella Tognola, Marcello Raspa, Paolo Gasparini, Giorgia Girotto
Publikováno v:
Redox Biology, Vol 19, Iss, Pp 301-317 (2018)
RedoxBiology 19 (2018): 301–317. doi:10.1016/j.redox.2018.08.002
info:cnr-pdr/source/autori:Anna Rita Fetoni; Veronica Zorzi; Fabiola Paciello; Gaia Ziraldo; Chiara Peres; Marcello Raspa; Ferdinando Scavizzi; Anna Maria Salvatore; Giulia Crispino; Gabriella Tognola; Giulia Gentile; Antonio Gianmaria Spampinato; Denis Cuccaro; Maria Guarnaccia; Giovanna Morello; Guy Van Camp; Erik Fransen; Marco Brumat; Giorgia Girotto; Gaetano Paludetti; Paolo Gasparini; Sebastiano Cavallaro; Fabio Mammano/titolo:Cx26 partial loss causes accelerated presbycusis by redox imbalance and dysregulation of Nfr2 pathway/doi:10.1016%2Fj.redox.2018.08.002/rivista:RedoxBiology/anno:2018/pagina_da:301/pagina_a:317/intervallo_pagine:301–317/volume:19
Redox Biology
RedoxBiology 19 (2018): 301–317. doi:10.1016/j.redox.2018.08.002
info:cnr-pdr/source/autori:Anna Rita Fetoni; Veronica Zorzi; Fabiola Paciello; Gaia Ziraldo; Chiara Peres; Marcello Raspa; Ferdinando Scavizzi; Anna Maria Salvatore; Giulia Crispino; Gabriella Tognola; Giulia Gentile; Antonio Gianmaria Spampinato; Denis Cuccaro; Maria Guarnaccia; Giovanna Morello; Guy Van Camp; Erik Fransen; Marco Brumat; Giorgia Girotto; Gaetano Paludetti; Paolo Gasparini; Sebastiano Cavallaro; Fabio Mammano/titolo:Cx26 partial loss causes accelerated presbycusis by redox imbalance and dysregulation of Nfr2 pathway/doi:10.1016%2Fj.redox.2018.08.002/rivista:RedoxBiology/anno:2018/pagina_da:301/pagina_a:317/intervallo_pagine:301–317/volume:19
Redox Biology
Mutations in GJB2, the gene that encodes connexin 26 (Cx26), are the most common cause of sensorineural hearing impairment. The truncating variant 35delG, which determines a complete loss of Cx26 protein function, is the prevalent GJB2 mutation in se